Neurogenic hypertension associated with an excessively high excretion rate of catecholamine metabolites.

Abstract

A 60 year old hypertensive patient suffered several cerebral infarctions. A phaeochromocytoma was suspected because the excretion rates of vanillylmandelic acid and its methoxy derivatives were raised and the patient had hypertensive crises. No tumour was found, however, by 131mI-iodobenzylguanidine scintigraphy and computed tomography of the abdomen. Moreover, the enhanced orthostatic plasma catecholamine response suggested that the high excretion rates of catecholamine metabolites were more likely to be caused by the syndrome of raised catecholamines after cerebrovascular accidents than a phaeochromocytoma. A phaeochromocytoma should not be diagnosed within several months of cerebral infarction without first excluding the possibility of a hyperadrenergic state induced by cerebral infarction.

Brain Stem Stroke Causing Baroreflex Failure and Paroxysmal Hypertension

“…18 Medullary stroke associated with paroxysmal neurogenic hypertension has been previously reported, but the exact anatomic location of the infarcts and the mechanisms involved were not demonstrated. 19,20 Animal studies have demonstrated that baroreceptor afferents, carried by the ninth and tenth cranial nerves, terminate in the nucleus tractus solitarius, a paired nuclear structure lying dorsally in the rostral medulla oblongata. 17 Inhibitory pathways extend to the rostral ventrolateral medulla, the tonic vasomotor center of the brain.…”